Cited by 846Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

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Obesity, inflammation and the immune system

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de Heredia, Fátima Pérez, Gómez-Martínez, Sonia, Marcos, Ascensión·2012·Proceedings of the Nutrition Society

DOI 10.1017/s0029665112000092

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Abstract

Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. The chronic inflammatory response has its origin in the links existing between the adipose tissue and the immune system. Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.

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Authors: de Heredia, F. P., Gómez-Martínez, S., & Marcos, A.
Affiliations: Consejo Superior de Investigaciones Científicas (ES)
Venue: Proceedings of the Nutrition Society
Publisher: Cambridge University Press (CUP)
Published: 2012-03-20
Volume: 71
Issue: 2
Pages: 332-338
ISSN: 0029-6651 (ISSN-L)
1475-2719
DOI: 10.1017/s0029665112000092
OpenAlex: W2001652786
Cited by: 845
References: 52
Citations by year: 2026: 32 · 2025: 97 · 2024: 87 · 2023: 94 · 2022: 92 · 2021: 86 · 2020: 65 · 2019: 47 · 2018: 44 · 2017: 35 · 2016: 39 · 2015: 37 · 2014: 39 · 2013: 40 · 2012: 10
FWCI: 5.07
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.cambridge.org/core/terms (unspecified)
Locations: Proceedings of The Nutrition Society (publishedVersion)
PubMed (publishedVersion)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords: obesity, chronic inflammation, leptin, adiponectin, free fatty acids, Toll-like receptors, adipokines, endoplasmic reticulum stress, hypoxia, visceral adipose tissue, abdominal obesity, immune function, metabolic disorders, children and adolescents
MeSH terms: Adipose Tissue, Hypoxia, Endoplasmic Reticulum, Fatty Acids, Humans, Immune System, Inflammation, Obesity, Overnutrition, Adipokines, Endoplasmic Reticulum Stress

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